Exam 3 Flashcards
1
Q
Where are micrococcus and Staphyloccus commonly recovered from?
A
From the environment or as commensals inhabiting skin and mucus membranes
2
Q
Key characteristics of Staphylococci
A
- Gram-positive
- Grape-like clusters
- Non-motile
- Non-spore-forming
- Catalase positive
- Usually facultative anaerobes
3
Q
Staph Aureus cluster pattern and color
A
- Grape like clusters
- Creme (or golden brown)
4
Q
Staph Aureus Habitat
A
- External environment
- Skin and mucous membranes
- 20-40% in the anterior nares
5
Q
Factors predisposing to serious infection with Staph Aureus (8)
A
- Defects in leukocyte chemotaxis
- Defects in opsonization by antibodies
- Defects in intracellular killing of bacteria due to inability to activate the membrane bound oxidase system
- Skin injuries
- Presence of foreign bodies
- Infection with other agents (e.g. viruses)
- Chronic underlying disease
- Use of antibiotics to which S. aureus is not susceptible
6
Q
Signs of serious infection of Staph aureus (5) + examples
A
- Pyoderma
- Furuncle (boils)
- Carbuncle
- Toxin-Mediated Infections
- Scalded skin syndrome
- Toxic-shock syndrome
- Food poisoning
- Disseminated Infections
- Osteomyelitis
- Endocarditis
7
Q
Staph Aureus Virulence Factors
A
- Capsules
- Protein A
- Panton-Valentine Leukocidin (PVL) (enzymes that alters cation permeability leading to white cell destruction)
- Coagulase
- Hemolysins (alpha, beta, delta, gamma)
- Toxins (exfoliatins, enterotoxins, enzymes)
- Superantigens (TSST-1)
8
Q
Delta-hemolysin
A
Virulence factor of Staph Aureus.
Produced by 97% of S. aureus. Acts as surfactant that disrupts the cell membrane, interacts with the membrane to form channels that increase the size resulting in leakage of cellular contents.
9
Q
What causes scalded skin syndrome?
A
Staph Aureus have exfoliatins/ epidermolytic toxins that dissolve the mucopolysaccharide matrix of epidermis, causing separation of skin layers
10
Q
What is responsible for the clinical features of staphylococcal food poisoning?
A
Entertoxins
11
Q
Superantigens (+ types (3)+ biological characteristics in common (4))
A
Group of toxins known as pyrogenic toxin superantigens. These include:
- Toxic shock syndrome toxin-1 (TSST-1)
- Streptococcal pyrogenic exotoxins (SPE)
- Streptococcal superantigens
All possess 3 biologic characteristics:
- Pyrogenicity
- Superantigenicity
- Enhance lethal effects of minute amounts of endotoxin
- Induce polyclonal T-cell proliferation
12
Q
Key facts about Staph. Epidermis (Frequency of isolation? What is it associated with? What is virulence related to? Role of Biofilm?)
Coagulase + or - ?
A
- Most frequently isolated clincally signative coagulase-negative staphylococci
- Associated with infections of indwelling devices
- Virulence related to production of extracellular slime that promotes adherence to surgace of forign bodies (forming biofilm)
- Biofilm plays important role in protection from antimicrobial angents, therefore FULL REMOVAL OF INDWELLING DEVICE IS NEEDED FOR FULL INFECTION REMOVAL.
13
Q
Staphylococcus saphrophyticus
(What does it cause? What is its identification based upon?)
A
- Cause of acute urinary tract infection in young women
- 2nd most common cause of uncomplicated cystitis among women of college and child-bearing age
- Identification based on negative coagulase and resistance to novobiocin
14
Q
Staphylococcus Lugdunensis (key features + what is unique about it?)
A
- Colonizes human inguinal area
- Causes wide variety of human infections
- Only species that is both PYR and Orthine positive
15
Q
In hospitals, what is the most important reservoir of MRSA? Who can serve as the link between these populations?
A
Colonized or infect patients. Hospital personnel can serve as a link for transmission between colonized or infected patients.
16
Q
The (6) settings associated with CA-MRSA
A
- Sports participants
- Correctional facilities
- Military recruits
- Daycare and other institutional centers
- Newborn nurseries and other healthcare settings
- Men who have sex with men (MSM)
17
Q
Key gene of MRSA
A
The mecA Gene
It encodes for altered “penicillin-binding protein 2a”. Has decreased binding affinity for B-lactam antibiotics (e.g. penicillin). This is what makes them resistant.
18
Q
Disease Symptoms in which MRSA should be considered a differential diagnosis.
A
- Skin and soft tissue infections (boils, spider bites, and cellulitis)
- Sepsis Syndrome
- Osteomyelitis
- Necrotizing pneumonia
- Septic arthritis
- Necrotizing fasciitis
19
Q
MRSA Infection Prevention Methods
A
- Active Surveillance (test all patients)
- Contact precautions
- Cleaning
20
Q
Staphylococci vs Streptococci (Catalase, physical arrangment, media, temperature for growth, prefered atmosphere?)
A
Staphylococci:
- Catalase positive
- Cocci in clusters
- Grows in minimal media
- Grows best at 35-37 C
- Aerobic preference
Streptococci:
- Catalase negative
- Cocci in pairs/chains
- Requires complex media
- Grows best at 35-37 (same as staph)
- Prefers anaerobic/ CO2 atmosphere
21
Q
Catalase
A
Common enzyme found in nearly all living organisms exposed to oxygen. IT catalyzes the decomposition of hydrogen peroxide to water and oxygen. Important in protecting the cell from ROS’s
22
Q
The 3 classifications of Streptococci Hemolysis
A
- Beta- complete hemolysis
- Alpha- incomplete hemolysis
- Gamma- no hemolysis
23
Q
What bacteria is associated with Strep Lancefield Group A?
A
Streptococcus pyogenes
24
Q
What bacteria is associated with Strep Lancefield Group B
A
Streptococcus agalactiae
25
The (6) clinical manifestations of Streptococcus pyogenes infection
1. Acute Pharyngitis
2. Impetigo
3. Erysipelas
4. Scarlet Fever
5. Necrotizing Fasciitis
6. Toxic Shock-like Syndrome
26
Impetigo (characteristics + age of association)
* Associated with _S. pyogenes_ Infections
* Pustule with yellow crust which appears on face or extremities
* 2-5 y/o children
27
Erysipelas
* Spreading erythema with well demarcated edge on the legs (historically on the face)
* Associated with S. pyogenes infections
28
Scarlet Fever is a complication of _______ \_\_\_\_\_\_\_.
It is caused by ________ \_\_\_\_\_\_\_\_
Signs and Symptoms?
1. Complication of streptococcal pharyngitis
2. Casued by erythrogenic exotoxin
3. Rash
4. **Blanches, Sore throat, Bright Red "Strawberry" Tongue**
29
Necrotizing Fasciitis
Strep infection that occurs deep in the subcutaneous tissues and leads to extensive destruction of the muscle and fat (flesh-eating)
30
What bacteria is Toxic Shock-like Syndrome Associated with?
Usually group A strep
31
Puerperal Sepsis?
* Seen in women following delivery or abortion
* Organisms colonizing genital tract or from OB personell invade upper GU tract leading to toxic shockk-like syndrome, nec. fasciitis, etc.
32
Post-Streptococcal Sequelae (2)
1. **Rheumatic Fever**: Inflammatory disease 1-5 weeks after strep pharyngitis with reoccuring attacks. Characteristic cardiac lesions which can later lead to possible endocarditis. Associated with fever, carditis and polyarthritis.
2. **Acute Glomerulonephritis**: Occurs after skin/respiratory infection. Edema, hypertension, hematuria and proteinuria. Immune complexes often deposited in glomeruli.
33
Virulence Factors of Group A Streptococci (4)
1. Adherence (capsular polysaccharide)
2. Invasion of epithelial cells
3. Avoidance of opsonization and phagocytosis
4. Production of toxins/enzymes (3 distinct heat labile toxins called superantigens)
* Responsible for rash in scarlet fever
34
Treatment of S. pyogenes
* Penicillin/ ampicillin/ amoxacillin (drug of choice- **no resistance worldwide**)
* Cephalosporins
* Erythromycin
35
Streptococcus agalactiae
Role in neonatal disease and how is it prevented
GBS
Plays role in neonatal pneumonia, sepsis and meningitis. Maternal colonization of vagina or rectum exposes baby at delivery.
_Prevention_: Cultures should be taken at 35 to 37 weeks and penicillin/ampicillin is given prophylatically
36
Limitation of Group A Rapid Test
It has a decreased sensitivity, which makes it less accurate. You must follow it up with the culture to get the final word.
37
Isolation of a bovis group from the blood is associated with...
...patients with carcinoma of the colon
| (Cow Cancer Colon)
38
Species included in the Strep Milleri Group (3) and what is their role?
1. S. anginosus
2. S. constellatus
3. S. intermedius
Commensals, but can cause deep-seated pyogenic infections
39
Species included in Nutritionally Deficient Streptococci
1. Abiotrophia
2. Granulicatella
40
Identify the key morphologic/ virulent factors of S.pneumoniae
_Structural characteristics_: Gram positive; polysaccharide capsule; bile-susceptible; IgA protease
__
41
Most common cause of bacterial meningitis in the U.S.?
Highest rate of meningitis among children younger than 2 years?
Invasive Pneumococcal Disease caused by *s. pneumoniae*. (for both questions)
42
Phenotype of S. pneumoniae as determined in the lab
1. Gram +
2. Lancet-shaped cocci (elongated w/ slightly pointed curvature)
3. Usually diplococci (but not always)
4. Catalase negative
5. BIle soluble
6. Inhibited by Optochin
43
When cultured on blood agar, S. pneumoniae shows what type of hemolysis?
It is alpha hemolytic
44
The 2 main species of Enterococcus and their relationship to penicillin/ ampicillin
What is their general resistance?
1. *E. faecalis* (susceptible to pen/amp)
2. *E. faecium* (resistant to pen/amp)
Both are inherently reisistant to many commonly used antibiotics
45
The 3 most common infections caused by enterococci
What infection occurs rarely?
1. Mixed bacterial wound infections
2. Sepsis
3. Endocarditis
4. RARELY meningitis
46
Enterococci are intrinsically resistant to...
...all cephalosporins, aminoglycosides, and trimethoprim-sulfa
(CATs)
47
Basic Enterococcus Characterisitics (4)
1. Gram positive cocci in pairs and short chains
2. Alpha, beta or gamma hemolytic
3. Group D antigen pos.
4. PYR pos.
48
What are the two pathological species of Neisseria?
1. Meningitidis
2. Gonorrhoeae
49
General characteristics of enterobacteriaceae
1. Gram negative rods
2. Indigenous flora of GI tract
3. Colonize resp. tract of hospitalized patients
4. Grow rapidly aerobically/ anaerobically
5. Simple growth requirements
50
Key endotoxin affliated with enterobacteriaceae?
LPS
51
What part of LPS is responsible for its toxicity?
Lipid A-- the inner most region of LPS. Responsbile for the endotoxin abilities of enterobacteriaceae. The fragments of this are responsible for shock.
52
The 4 unwavering biochemical characteristics shared by all enterobacteriaceae.
1. Faculatative Gram-Neg rods
2. Ferment glucose
3. Reduce nitrate to nitrite
4. Oxidase negative
53
The most important species of Escherichieae
E. coli
54
E. coli habitat
Intestines of humans and animals (no where in the external enivronment)
55
Clinical Syndromes associated with E. Coli (6)
1. Gram negative sepsis
2. UTI's (80% of community acquired UTI's)
3. Wound infections
4. Pneumoniain IC hospitalized patients
5. Meningitis in neonates
6. Gastroenteritis
56
Name the five groups of E. coli that can cause gastroenteritis and the signs and symptoms of diarrheal disease that is produced by each group .
1. _Enterotoxigenic E. coli (ETEC)_- profuse watery diarrhea (traveler's)
2. _Enteropathogenic E. coli (EPEC)_- Infants. Mucusy diarrhea, but NO gross blood
3. _Enteroinvasive E. coli (EIEC)_- Blood, mucus and many leukocytes in stool
4. _Entero-Hemorrhagic E. coli (EHEC)_- Bloody diarrhea w/o WBCs. Produce shiga-like toxin (STEC)
5. _Enteroaggregative E. coli_ _(EAggEC)_- Watery diarrhea with blood and mucus
57
Shiga Toxin (STEC) is associated with what type of E. coli
Entero-Hemorrhagic E. coli (EHEC) --\> Primarily caused by E. coli O157:H7
58
Resevoir and Transmission of E. coli O157
* **Reservoir**: Healthy Dairy Cattle
* **Tranmission**: Food (usually ground beef), water, or direct contact with an infected patient
STEC is shed in the feces of cattle, sheep, deer, and other ruminants
59
Triad of symptoms for _Hemolytic Uremic Syndrome_
1. acute renal failure
2. thrombocytopenia
3. hemolytic anemia
60
Laboratory Diagnosis of Disease caused by Shiga-toxin (Timing, type and transport of specimen?)
What is used for the actual diagnosis?
* _Timing:_ Specimens are best collected early, when organism load is higher and before antibiotics
* _Type:_ Whole stool is preferred
* _Transport:_ As soon as possible. Refrigerate if more than 1-2 hours
Antigen detection or FilmArray GI Panel (Multiplex PCR) is used for the final detection.
61
Treatment of STEC diseases (how is the diarrhea treated? antibiotics or no? antimoltility drugs or no?)
_DIarrhea:_ Oral rehydration; HUS/ renal failuremanaged by dialysis; NO ANTIBIOTICS OR ANTIMOTILITY AGENTS (can increase HUS risk)
62
Strep Pneumo is the #1 cause for what (4) diseases?
MOPS
1. Menengitis
2. Otitis media
3. Pneumonia
4. Sinusitis
63
Shigella is very similar to E.coli but has some differences. What are the key id features of Shigella which sepearate it from E.coli? (3)
1. Non-lactose fermenter
2. Non gas producer
3. Nonmotile
64
What are the modes for shigella transmission?
Person to person via fecal oral route
Usually via contaminated...
1. water
2. 5 F's (food, flies, fingers, fomites and feces)
65
Who's at highest risk for Shigella Transmission? (3 groups)
1. Young children in day care center, nurseries, or custodial institutions
2. Siblings/parents of these children
3. Male homosexuals
66
Clinical manifestation of Shigella
**Bacillary Dysentery**
* _Signs and Symptoms_: Abdominal cramps; tenesmus (urge to poop but there is none); pus and blood in stool; Fecal leukocytes are present
67
What is the important species of Edwardsielleae?
Edwardseilla tarda (E. tarda)
68
Habitat for E. tarda (3)
Cold blooded vertebrates; fresh water; catfish
69
Main clinical syndromes associated with E. tarda (2)
What is it sometimes mistaken for?
1. Acute, self-limiting **Gastroenteritis** with watery diarrhea. Can develop to typhoid-like illness with bloody diarrhea and possible fever, nausea, comiting, colonic ulcerations and terminal ileum nodularity.
2. **Septicemia (rarely)**
Has been mistaken for salmonellosis and inflammatory bowel disease
70
Species and habitat for *Salmonella*
Lower animals (Poultry, cows, pigs, pets) for _non-typhoid strains_. Humans for _S. Typhi_.
****
All serotypes are considered a **single species**
71
The (5) characteristics of Salmonella
(lactose fermenter or non-fermenter? How does it plate on TSI? How is it transmitted?)
1. Non-lactose fermenter
2. Produces hydrogrn sulfide (black)
3. Transmission via improper food handling (**usually poultry/poultry products**; reptiles as well)
4. Found in humans and livestock
5. Secondary transmission person-to-person
72
The (5) _Clinical Syndromes_ of Salmonella
1. Asymptomatic (carrier) state
2. Febrile Gastroenteritis (\*\*Most common presentation\*\*)
3. Enteric Fever
4. Septicemia
5. Focal Infections (osteomyelitis, endocarditis, etc.)
73
What types of Salmonella cause enteric fever?
S. Typhi and S. paratyphi
74
What patients are most at risk for septicemia from Salmonella? (5 pt. types)
Patients with underlying:
* Leukemia/ lymphoma
* AIDS
* Lupus (SLE)
* sickle cell crisis
* alcoholic hepatitis
75
Key dermalogical sign of enteric fever
Rose spots (pink macules or prupuric lesions)
76
Clinical syndromes associated with *Citrobacter* (3)
Nosocomial infections of (1) urinary and (2) respiratory tracts of debilitated, hospitalized patients. Can also cause (3) endocarditis.
77
What are *C. freundii* and *C.* *koseri, *and what can they each cause?
Species of Citrobacter
_C. freundii_: rare cause of diarrhea
_C.koseri_: rare cause of meningitis and brain abscess in neonates
78
What are the 10 types of enterobacteriaceae?
1. E. Coli
2. Shigella
3. Salmonella
4. Edwardsiella
5. Citrobacter
6. Klebsiella
7. Enterobacter
8. Serratia
9. Proteus
10. Yersinia
79
What are the (3) Genuses under Klebsielleae?
1. Klebsiella
2. Enterobacter
3. Serratia
80
Nosocomial diseases
Diseases originating in the hospital
81
The (4) Klebsiella types and their associated clinical syndromes:
* (1.) **K. pneumoniae** and (2.) **K. oxytoca**: Primary lobar pneumonia characterized by destructive changes to lungs (necrosis, hemorage [jelly sputum], etc.) as well as UTI's
* (3.) **K. ozaenae**- atrophic rhinitis + destruction of mucosa
* (4.) **K. rhinoscleromatis**- rhinoscleroma, chronic granulomatous disease involving upper respitaroy tract
82
Clinical syndromes associated with enterobacter
Frequent colonizers of hospital patients, casuing opportunistic infections involving urinary tract, respiratory tract, and cutaneous wounds (occasional septicimeia and meningitis)
83
Most important species of and clinical syndromes associated with _Serratia_ ( 2 main groups of effects)
What color does it plate?
S. marcescens
(Produce red colonies)
_General Effects of enterobacteria:_ Nosocomial infections, pneumoniae, epticemia, etc.
_Also_ can cause endocarditis and osteomyelitis in IV drug addicts
84
The 2 most important species of Proteeae and the (2) ID features associated with them both.
P. mirabilis and P. vulgaris
(1) Swarming observed on blood agar (due to growth in spurts) and (2) strongly urease positive
85
Proteus Clinical Syndromes (Syndromes for P. mirabilis? Syndromes for P. vulgaris)
_P. mirabilis_: most frequently isolated (second only to E. Coli). Cause of UTI and wound infections. Alkaline urea (due to urease) can lead to renal calculi (kidney stones from struvite-- staghorns).
_P. vulgaris_: most commonly recovered from infected sites in IC patients
86
Key Lab ID feature of Yersinia enterocolitica
What is the main reservoir associated with Y. enterocolotica
Pinpoint colonies on MacConkey at 24 h
Pigs are a major reservoir for human infection (chitterlings).
87
Clinical syndromes associated with Yersinia enterocolitica
Associated with diarrheal disease and acute enterocolitis. Can mimic appendicitis.
Also associated with transfusion related sepsis and infections, as it can proliferate in blood stored at 4 degrees C, after 2-3 weeks.
88
Name the five genera of Enterobacteriaceae that can cause gastrointestinal disease.
1. E. coli
2. E. tarda (Edwardsiella)
3. Citrobacter (C. freundii)
4. Salmonella/Shigella
5. Y. enterocolitica
89
(7) Key structural/cultural characteristics used by both Neisseria forms
1. Gram-negative
2. Kidney bean diplococci
3. LPS
4. Pili
5. Required enriched media (VPN or Chocolate agar)
6. Oxidase positive
7. Glucose consumption
90
What is the difference in sugar oxidation between N. gonorrhoeae and N. meningitidis?
Although they both oxidize glucose only menigitidis oxidzies maltose.
91
6,000- fold increaase risk for meningococcal and disseminated gonococcal disease in persons with deficiency of...
One or more of the terminal components of _Complement_ (C5-9)
92
Key virulent components of Neisseria meningitidis:
1. Polysaccharide capsule
2. LOS (N. meningitidis version of LPS): responsible for cell damage and systemic inflammation
93
Main (2) clinical manifestations of Neisseria meningitidis infection + presentation for each
What is another key manifestation?
1. Meningococcemia (shock; hemorrhage; purpura; adrenal hemorrhage)
2. Meningitis (headache; AMS; neurological signs; skin petecheae/purpura)
Urethritis
94
What culture results make you lean towards Neisseria meningitidis as a diagnosis?
1. Oxidase positive
2. Oxidation of glucose
3. Oxidation of maltose
4. Growth on nonselective media (blood or chocolate agar)
5. Growth enhanced in CO2
95
Neisseria meningitisis treatment (2)
Penicillin (resistance is uncommon); ceftriaxone can also be used and it cross BBB
96
What drugs are used for chemoprophylaxis for household contacts of individuals diagnosed with Meningitis? (3)
1. Rifampin
2. Ciprofloxacin
3. Ceftriaxone (1 dose)
97
The 4 key antigenic structures of Neisseria gonorrhoeae + their location
1. Pili (adhesion)
2. PorB (Pores which facilitate epithelial cell invasion)
3. Opa (adherence proteins)
4. Rmp proteins (stimulate blocking antibodies)
All located in the outer membrane
98
Gonorrhea is a [intracellular/ extracellular] pathogen
INTRACELLULAR.
Tends to invade PMNs
99
Location where N. Gonorhea use Pili? Opa proteins?
_Pili_: urethral and vaginal epithelium, nonciliated fallopian tube epithelium, sperm, neutrophils
_Ops proteins_: cervical and urethral epithelium and other gonoccocal cells
100
Most common sign of localized gonorrhea for men (in general)? For women? For gay men?
Men: Urethritis
Women: Cervicitis
Gay Men: Prostatitis
101
Most common manifestations of disseminated gonorrhea
Pelvic Inflammatory Disease (women); Arthritis
102
What is the main clinical specimen used for direct detection for gonorrhea clinical specimens?
Nucleic acid amplification of a _urine specimen_
103
What drugs are used for treatment of Gonorrhea?
Ceftriaxone- single dose (NO ORAL TREATMENT!)
**_PLUS_** azrithromycin (single dose) or Doxycycline (7 days) for _co-infection with Chlamydia_
104
N. Gonorrhea and Penicillin
Usually Gonorrhea is penicillin resistant due to PBP and B-lactamase (PPNG) alterations
105
What gram type is haemophilus? Where is it found? Capsule or no Capsule?
Encapsulated gram-negative coccobacilli found in the respiratory tract.
106
Main capsule type for Haemophilus influenzae
Type B
107
Haemophilus influenzae type b: Clinical Manifestations (4)
Nontypable H.I. manifestations (3)
1. Meningitis
2. Epiglottis (cherry red epiglottis)
3. Cellulitis
4. Arthritis
(usually in young children around 2-4)
_Non-typable:_
Otittis media
Sinusitis
Bronchitis
108
Lab Diagnosis of Haemophilus influenzae
(Gram stain of what? Cultrue type? Motility? Spore-formation? Growth factors?)
* _Gram stain_- CSF, joint fluid
* _Culture_- chocolate agar
* Nonmotile, non-sporeforming
* **Require growth factors from lysed blood**
* X factor (hematin) "hema-TEN"
* V factor (NAD) "N = nickle"
109
25-50% of Haemophilus influenzae is resistant to _______ because of the production of \_\_\_\_\_\_\_.
Ampicillin
Beta-lactamase
110
Haemophilus influenza vaccine is often conjugated to what things? (3)
1. Diphtheria toxoid
2. N. memingitides OMP
3. Tetanus toxoid
111
Bordetella pertusis is aka...
Whooping cough
112
Is Bordetella pertusis Gram + or - ?
Negative
113
What are the 4 main toxins associated with Bordetella pertusis?
- Pertussis toxin (PT)
- Tracheal cytotoxin (peptidoglycan fragment)
- Dermonecrotic toxin (causes ischemic necrosis)
- Endotoxin (LPS)
114
What are the 2 main adhesin types associated with Bordetella pertusis?
Pertactin and Filamentous hemagglutinin (Fha)
115
Mechanism of action (2) of Pertussis Toxin and clinical manifestations
Made from AB subunit
* "A" catalyzes ADP ribosylation of a G-protein, preventing inactivation of adenylate cyclase, leading **increased respiratory secretions, mucus production and _lymphocytosis_**
* "B" binds to receptors on ciliated respiratory cells and phagocytic cells
116
Adenylate Cyclase Toxin
Affliated with Bordetlla Pertussis
Causes increase cAMP levels in cells affecting leukocyte function
117
Who often acts as the reservoir for Bordella pertussis?
Adults because they don't classic symptoms
118
The 4 stages of Bordella Pertussis and what occurs at each stage
1. **Incubation**
2. **Catarrhal** (Rhinorrhea, malaise, fever, sneezing, anorexia)
3. **Paroxysmal** (coughs w/ whops, vomiting, leukocytosis)
4. **Convolescent** (diminished cough, development of secondary complications)
119
Main method used for B. Pertussis ID in lab
PCR
120
What is used in treatment of Bordetella pertussis? What effect does this have on the disease state/ epidemiology?
Azithromycin is effective in early disease.
It eliminates nasopharyngeal organisms and prevents spread but it _does not alleviate the cough_.
121
What vaccines are recommended for Bordetella pertussis (2)?
1. DTaP for all children
2. Tdap for all adults
122
Pseudomonas aeruginosa habitat
* Environmental organism
* Grows in moist, unsterile areas (cut flowers, hot tubs, toilets, mops etc.)
123
Describe the type of patients who acquire Pseudomonas aeruginosa infections (4)
1. Burn Patients
2. Cystic fibrosis patients
3. Patients with hematologic malignancies
4. Immunocompromised patients
124
List the major toxins produced by Pseudomonas aeruginosa and describe their principle effect on human cells (3)
1. **Exotoxin A:** Blocks protein synthesis, contributing to dermatonecrosis in wounds and tissue damage in lungs
2. **Exoenzyme S:** ADP-ribosylating toxin. Epithelial cell damage facilitates bacterial spread, tissue invasion and necrosis
3. **Elastase:** Results in tissue destruction and hemorrhagic lesions (ecthyma gangrenosum). Las A nd Las B enzyymes act synergistically to degrade elastin . Degrades compliment components and inhibits neutrophil chemotaxis and function.
125
List the diseases associated with Pseudomonas aeruginosa (9)
1. Folliculitis (hair follicle infection)
2. Nail Infections
3. Severe necrotizing bronchopneumonia
4. UTIs
5. Ear infections (swimmers ear)
6. Eye infections
7. Bacteremia (Ecthyma gangrenosum)
8. Endocarditis (IV Drug Users)
9. Osteomyelitis
126
Ecythyma gangrenosum
–EG is a well-recognized but uncommon cutaneous infection most often associated with a Pseudomonas aeruginosa bacteremia.
–EG usually occurs in patients who are critically ill and immunocompromised and is almost always a sign of pseudomonal sepsis.
127
Diagnosis of P. aeruginosa (culture type/appearance; ID characteristics)
* Grows on blood and MacConkey agar producing colonies with metallic sheen
* Green colored
* Grape-like odor
* Oxidase positive
* Grows at 42 degrees C
128
Name the non-fermenters that are named on the biothreat agent list
1. Burkholderia pseudomallei
129
Burkholderia pseudomallei Melioidosis can present itself in what 3 ways?
1. **Acute disease** (septicemia + metastatic lesions) 95% mortality
2. **Subacute disease** (most common). TB like pneumonia with cellulitis and lymphangitis
3. **Chronic Disease:** Localized chronic cellulitis. Treated with antibiotics prior to draining otherwise becomes bacteremic.
130
Discuss the association of Burkholderia cepacia and pulmonary infection in cystic fibrosis patients
Mutation in CFTR results in defects in innate immunity, increased airway inflammation and sticky mucus which provides an ideal niche for chronic lung infection. Chronic lung infection accounts for 85% of deaths with CF and _B. cepacia_ is one of the top pathogens that lead to infection (along with S. aureus and P. aeruginosa)
131
What is pulmonary exacerbation?
Cellular defect from CF results in increased mucus thickness and thus impaired innate immunity within lungs. This leads to exacerbation by recruitment o neutrophils, cytokines and neutrophil elastases which cause signficant lung pathology.
132
Burkholderia cepacia is affliated with what disease types?
Respiratory tract infections (major issue for patients with CF); UTIs; Septicemia
133
Main disease associated with Burkholderia pseudomallei
Melioidosis
134
Diseases associated with Stenotrophomonas maltophilia
Where is S. maltophilia usually aquired?
* Opportunistic infections (bacteremia, UTI's, etc.)
* Usually respiratory infections
Usually hospital acquired and causes systemic infections in debilitated patients because it is very resistant to antibacterials
135
What is unique about the growth of S. maltophilia?
It is a non-fermenter that is _oxidase negative_.
136
Diseases associated with Elizabethkingia meningoseptica?
Location?
Resistance?
1. Associated with neonatal meningitis
2. Pneumonia in adult (usually IC) patients
Usually nosocomial. Outbreaks traced to breast pumps used in hospital nurseries
Very Resistant
137
Diseases associated with Acinetobacter baumannii
Implicated in community acquired and nosocomial infections
138
Key identifying characteristics of Bacillus (4)
Is it motile? Any exceptions?
1. Spore forming Gram positive rod
2. Widespread in nature
3. Prefers aerobic conditions
4. Motile except for B. anthracis
139
Epidemiology of Bacillus anthracis (biothreat category, spread)
* Category A biothreat agent
* Spreads via:
* _Inoculation_ (95%): contaminated soil or infected animal products
* _Inhalation_: Wool sorters disease; processing goat hair; **biological weapons**
* _Ingestion_
*
140
Clinical presentation of Bacillus anthracis
1. **Necrotic eschar**
2. **GI anthrax**: Upper GI: ulcers in mouth/esophagus; Lower GI: N/V malaise, bloody diarrhea
3. **Inhalation Anthrax:** Initial symptoms are nonspecific (flu-like); second stage symptoms include edema and enlargment of mediastinal lymph nodes (_accounting for widened mediastinum observed on chest X-ray)_
141
Key toxins of Anthrax
Edema Toxin and Lethal Toxin
142
The 3 distinguishing biochemical markers of anthrax
1. Motility negative
2. Non-hemolytic
3. PCN susceptible
143
The 3 forms of anthrax disease
1. Inhalation
2. GI
3. Cutaneous
144
Name the 2 aerobic Gram-positive rods that can cause food poisoning
1. Bacillus cereus
2. Listeria
145
Describe the key ID characteristics of Listeria monocytogenes (7\*)
(\*3 of them are motlity related)
(spore-forming? Gram-staining? Where does it live? Catalase? Motility?)
1. Non-spore forming
2. Gram-positive rod
3. Can live in animals and refrigerated foods
4. Catalase +
5. Tumbling motility
6. Umbrella motility
7. Motile at root temp
146
ActA gene and Listeria
ActA gene is utilized to move bacteria into adjacent cells without exposure to immune system by using the actin of cells
147
Explain why patients with defects in cellular immunity are particularly susceptible to infections with Listeria monocytogenes and list three patient populations that are at risk for listeriosis (+ what happens to them?)
Listeria moves from cell to cell so is rarely ever exposed enough for antibodies (humoral response) to have a major effect.
Neonates (early granulomas, late menigitis) Elderly (flu-like + or - gastroenteritis) and Pregnant women/ patients with cell-mediated immune defects (bacteremia or disseminated disease with hypotension/meningitis) are most at risk.
148
Key identifying characteristics of Erysipelothrix rhusiopathiae (5)
(what does it look like? aerobic or anaerobic? Growth speed? hemolysins? Production on TSI?)
1. Pleomorpic gram postive rods that form long filaments ("hairlike")
2. Facultative anaerobe
3. Slow growth (2-3 days incubation)
4. Small, grayish, _alpha-hemolytic_ colonies
5. Produces H2S on triple sugar iron (TSI) agar
149
Epidemiology of E. rhusiopathiae
1. Ubiquitous in soil and groundwater
2. Widely recognized in animals but human disease is uncommon
3. Human infection is aquired from occupational working with animals (butcher, vet, etc.)
150
Diseases associated with E. rhusiopathiae (2)
Cutaneous infections after subcutaneous inoculation
Two forms:
1. _Erysipeloid_: localized skin infection on fingers/ hands. Slowly spreads peripherally
2. _Septicemic_: uncommon; frequently associated with endocarditis
151
Characterisitcs of Corynebacterium
1. gram positive rods
2. clumps of organisms resembling chinese letters
3. Commonly called "diphtheroids"
152
Epidemiology of Corynebacterium? (location, spread, etc.). What are the important species?
_Location_: Colonize skin, upper respiratory tract, GI tract, GU tract
_Spread_: infection transmitted by respiratory droplets or direct contact with cutaneous infection (rare in US due to vaccine)
_Important Species_: C. diphtheriae; C. jeikeium
153
Clinical manifestation of Corynebacterium diseases (what do the toxins inhibit? where can they circulate? what does it lead to?)
Disease caused by potent exotoxin which inhibits protein synthesis.
Leads to _pharyngitis with patchy exudates_ on tonsils, uvula and soft palate (leathery skin). Toxins can circulate to the CNS or heart causing injury.
154
C. jeikeium and resistance
A species of Corynebacterium.
Infects immunocompromised patients. Resistant to most antibiotics (except vancomycin)
155
Characteristics + key clinical manifestion of Arcanobacterium hemolyticum (what does it cause? Who is it isolated from?)
* Beta-hemolytic (similar to group A Strep)
* Isolated mostly from young adults
* curved, club-shaped or "V" formation Gram-positive rod
Appears very similar to group A strep
Causes fever, rash, pharyngitis. Isolated from wounds/ blood of patients with septicemia and endoarditis.
156
Main difference between Listeria and Strep
Listeria is _catalase +_
157
Key characteristics of Nocardia species (gram-positive or negative? Aerobic or anaerobic? Incubation? Cell wall? Best stain for it?) (5)
1. Gram-positive
2. Cell wall with mycolic acid
3. Strict aerobe
4. Prolonged incubation
5. Partial acid-fast
Type of actinomycete
158
Epidemiology of Nocardia? Who is the disease most common in?
Worldwide distribution in soil. Infection via inhalation or traumatic introduction.
Disease most common in pts with chronic pulmonary disease or immunocompromised pts. with T-cell deficiencies
159
Diseases associated with Nocardia (3)
1. Pulmonary disease
2. Primary or secondary cutaneous infections
3. Secondary CNS infections
160
Diseases associated with Rhodococcus
1. Pulmonary diseases
2. Opportunistic infection (wounds, peritonitis, etc.)
161
Disease associated with Tropheryma
Whipple's Disease
162
_Pathogenicity of Treponema pallidum_
Visble in light Microscopy?
Vector/ Reservoir?
Transmission?
Disease?
**Visble in light Microscopy**: No (darkfield is best)
**Vector/ Reservoir**: None
**Transmission**: Intimate sex/ contact
**Disease**: Syphilis
163
_Pathogenicity of Leptospira interrogans_
Visble in light Microscopy?
Vector/ Reservoir?
Transmission?
Disease?
**Visble in light Microscopy:** No (darkfield is best)
**Vector/ Reservoir: **Rodents, dogs, swine, cattle
**Transmission:** Contact or ingestion of urine-contaminated water
**Disease:** Leptospirosis
164
_Pathogenicity of Borreli recurrentis_
Visble in light Microscopy?
Vector/ Reservoir?
Transmission?
Disease?
**Visble in light Microscopy:** Yes
**Vector/ Reservoir:** Lice, ticks, rodents
**Transmission:** Ticks or lice
**Disease:** Relapsing fever
165
_Pathogenicity of Borrelia burgdorferi_
Visble in light Microscopy?
Vector/ Reservoir?
Transmission?
Disease?
**Visble in light Microscopy:** Yes
**Vector/ Reservoir: **Ticks, mice, deer
**Transmission: **Ticks
**Disease:** Lyme disease (lyme borreliosis)
166
Describe the pathogenesis of Syphilis infection (how does it enter the body? when symptoms begin? describe the pathogenic lesion?)
- passes through _intact mucosa or abraded skin_
- **symptoms** occur when number of organisms reach critical mass (10-90 days post inoculation)
- **pathogenic lesion** is obliterative endarteritis (leading to blockage of arterial vessels)
167
Describe the presentation of primary syphilis
An ulcerative lesion at site of inoculation (**chancre**) with _regional_ adenopathy (node enlargment). Heals spontaneously.
168
Describe the presentation of secondary syphilis
Systemic flu-like illness which may develop 2-10 weeks after primary lesion heals. Fever, papulosquamous rash and _generalized_ lymphadenopathy along with spread to almost all local sites.
169
How does congenital syphilis present at birth? Later in life?
The child is actually _normal at birth_.
Multisystem diseases occur later in life inlcuding rhinitis (nasal snuffling), rashes, issues with bone and cartilage involvement (teeth) and CNS, liver and spleen issues.
170
The two types of tests which lead to a diagnosis of Syphilis
_Nontreponemal Tests:_ Not specific to just syphilis. Screens for antibodies against cardiolipin (which is part of T. palidum) "Venereal Disease Research Laboratories (VDRL)" or "RPR"
_Specific Treponemal Serology Tests_: Measure specific antibody against T. pallidum (ex. Fluorescent Treponemal Antibody- Absorption Test (FTA-Abs or TPPA (MHA-TP))
171
Treatment of Syphilis
It's extremely sensitive to penicillin
172
Jarisch-Herxheimer Reaction
Caused during death of T. pallidum
Release of toxic products from killed spirochetes. Causing fever, chills, headache and hypotension.
173
What is the mechanism for relapsing fever?
B. recurrentis and related organisms escape immune recognition by altering their antigenic structure during infection (S and E segments)
Resolves in 3-5 days, remits after 7-9 days. Each relapse is less severe.
174
What are the (2) primary reservoirs for lyme boreliosis (borrelia bergdorferi)? What spreads it?
Deer and white footed mouse --\> reservoirs
Spread by tick
175
Clinical manifestation of Lyme Disease (early, early disseminated, late)
_Early_: erythema migrans (bulls-eye rash); flu-like symptoms
_Early Disseminated_: fatigue, headache, fever, malaise, neuropathies (**facial nerve paralysis**), heartblock
_Late_: Arthritis; Encephalopathy (memory loss, cognitive defects, etc.)
176
How is Leptospirosis acquired?
A zoonosis affecting a variety of animal species. Humans acquire the organism by contact with _infected animal urine_, usually through contaminated _water_ (often water sports)
177
Leptospirosis pathogenesis
After infection, spirochetes invade bloodstream and _affect endothelial cell integirty_ causing vasculitis in many organs. **Immune complexes found in kidney.**
178
Clinical Manifestations of Leptospirosis (3 stages)
_First Stage_ (bacteremia- bug in blood): fever, headache, conjunctival suffusion
_Second stage_ ( immune- bug no longer in blood/CSF, only urine): aseptic memningitis or generalized illness with headache, rash, etc.
_Severe_: (stages blend) Prominent hepatitis, kidney involvment, hemorrhage
179
How does Treponema pallidum move?
Axial fibril (internal flagellum)
180
Syphilis and self-limitation
Primary and secondary stages of lymphocytes are self-limiting
181
Natural History of Untreated Syphillus
1/3rd of pts _resolve_ the infection
1/3 convert to _latent_
1/3rd go to _tertiary syphilis_ (neuro, cardiovascular, gummatous)
182
List the animal vectors associated with:
Brucellosis
Plague
Tularemia
Pasteurellosis
**Brucellosis**: Goats, sheep, camels, pigs, cattle, dogs
**Plague**: Fleas, rodents/small animals
**Tularemia**: Voles, Lagomorphs (rabbits), ticks, deer flies, mosquitoes
**Pasteurellosis**: All types of animals but especially _cats_ and _dogs_
183
Human populations at risk for Brucellosis
What level of Bioterrorism Agent is it?
1. Those who consume unpasteurized dairy products
2. Contact with infected animals (slaughterhouse workers, vets, farmers)
3. Lab workers
Category B Bioterrorism Agent
184
Describe the disease conditions associated with infections caused by Brucella (basic pathogenesis, clinical manifestations (initial + advanced)
_Pathogenesis_: Organisms are phagocytized by macrophages and carried to spleen, liver, etc. Host forms small granulomas and pathogen survives within cell.
_Clinical Manifestations_: **Initial** is non-specific (flu-like); Unudulant fever (fever of unknown origin [FUO]); splenomegaly, hepatomegaly, etc.; **Advanced**: GI issues, Osteolytic lesions, respiratory symptoms.
185
Key culture characterisitics of Brucella (size, shape, gram status, growth speed, media)
* Small coccobacillary Gram negative rod.
* Slow growing
* Requires enriched media (chocolate agar) to grow and prolonged incubation
186
Describe the populations at risk for Zoonoses caused by Francisella tularensis and identify within the USA where tularemia is endemic.
Is there a vaccine available?
Hunters, lab workers, people exposed to ticks. Most patients are men (because men hunt more often)
Parts of US where endemic: Arkansas, Ohlahoma, and Missouri
Vaccine? Yes
187
Describe the disease state associated with Tularemia (pathogenesis + clinical manifestations( 5))
Where is this on the biothreat list?
_Pathogenesis_: Organsims enter through breaks in the skin and an **ulcer** may develop at the entry site. Organisms disseminate via bloodstream and host response is **granuloma** formation. **Facultative intracellular organism.**
_Clinical Manifestations_: Usually **ulceroglandular** (papule at site that is necrotic and ulcerates). Could be **oculoglangular**, **typhoidal**, **pneumonic infection**, **_glandular (adenopathy)_, oropharyngeal** --\> all depends on method of exposure
Category _A_ biothreat
188
Culture characterisitcs of Francisella tularensis. (size, shape and gram status? aerobic vs anaerobic? media? Color? Incubation period? )
* Very small gram-negative coccobacilli
* Cannot be isolated on routine media (_requires cystein supplemented media_). Can also be recovered on chocolate agar and charcoal yeast extract (CYE)
* Strict aerobe
* Pearly white colonies with slight greening of agar below
* Long incubation (up to 3 weeks)
189
Describe the disease state associated with pasteurella (how its spread and clinical manifestations)
_Spread_: Associated with cat and dog bites/scratches. May be aquired by respiratory route.
_Clinical Manifestations_: Painful swelling, redness, cellulitis. If the wound is very deep _septic arthritis, osteomyelitis_ or even _fasciitis_ (in compromised hosts) can occur.
190
Culture characteristics of Pasteurella multocida (size, shape, aerobicity, media, odor, oxidase status, catalase status)
Small bipolar Gram negative rods
Facultative anaerobe
Grows on blood and chocolate but _not_ MacConkey
Large "buttery" colonies w/ moth ball odor
Most species are _oxidase-positive_ and catalase-positive
191
Epidemiology of the plague (The 2 endemic forms and how it spreads)
What category bioterrorism agent is it?
_Two endemic forms_: **Urban Plague__**__- maintainted in rat pop.. Spread to humans by fleas. **Sylvatic Plague-endemic** ( _western USA)_. Carried by prairie dogs, mice, rabbits and rats.
Often times spread to human by domestic cats or otherwise fleas
_Category A bioterrorism agent_
192
Disease state of Plague (pathogenesis + clinical manifestations for each plague type (3) )
_Pathogenesis_: Facultative intracellular organisms; causes enlarged tender lymph nodes with hemorrhagic necrosis (black buboes); _terminal cyanosis_ (Black death)
_Clinical Syndromes_: ****
1. **Bubonic Plague**: Fever + painful bubo days after bite; fever chills, weakness and intense pain
2. **Septicemic Plague**: Direct infection of bloodstream; fever, delirium, seizures, septic shock; Black hemorrhagic splotches (Black death)
3. **Pneumonic Plague**: plague bacillus reaches lung. Respiratory signs of infection (cough, chest pain, hemoptysis, infectious sputum)
193
Culture characteristics of _Yersinia pestis_ (plague) (oxidase, size and shape, speed of growth)
oxidase negative; cells look like safety pins (small, cocco-bacillary); small pinpoint coloneysin 24 hours ( but fried egg under microscope if left out); slow growing on ordinary media
194
Is there a vaccine for Yersinia pestis?
Yes; only for high risk patients
195
Unusually fact about Pasteurella treatment
It is very susceptible to penicillin, which is unusually because it is gram-negative (which tends to put up a bigger fight to penicillin due to the outer wall)
196
Staining for rickettsii
Giemsa
197
Why is rickettsia an obligate intracellular?
It requires host NADP+, COA, and ultimately ATP in order to function
198
Why is coxiella not killed when a phagosome containing it fuses with an endosome?
Coxiella actually requires a slightly lower pH, so fusion with a phagosome promotes its function
199
Which rickettsia does not migrate using actin polymerization?
R. Prowazekii
200
What causes the red rashes affliated with the ricketsia's?
Bacteria multiply in endothelial cells lining small blood vessels. Rupture results in rash and primary lesion (vasculitis)
201
Cause and clinical manifestation of Rocky Mountain Spotted Fever
Rickettsia rickettsii (intracellular; replicates in cytoplasm and spreads via actin polymerization)
_Syndromes_: Rash on extremities, high fever, headaches
202
Epidiemiology of Rocky Mountain Syndrome (vector, time of transmissionwhen is it most common, where is it most common)
_Vector_: Hard **ticks** (dog, wood) are vectors; transmission requires prolonged contact.
_When_: most common in summer
_Where_: Southeast atlantic, south central states
203
What is the cause for Rickettsialpox? What are the clinical manifestations? Describe the two phases.
How is it resolved?
Rickettsia akari
_Clinical Manifestations_: Mild disease with vesicular rash; self limiting
_2 phases:_ **phase 1:** firm red papule at site of bite which develops into vesicle then black eschar as bacteria spread. **phase 2**: high fever, headache, myalgias, photophobia etc.
Self-limiting after 1 week; no deaths reported
204
Epidemiology of Rickettsialpox (vector, where is it found?)
Vector is bloodsucking mites, found on mice
Found in northern USA, Russia, Africa, Korea
205
Cause of Epidemic typhus? Clinical manifestations?
Rickettsia prowazekii
_Manifestations_: Fever, headache, myalgias; _maculopapular rash_ (first on the trunk then spreads to extremities)
206
Epidemiology for Rickettsia prowazekii (location, spread, reservoir, vector)
* Present in central and south america, and africa
* Disease associated with unsanitary conditions (peaks in winter)
* Tranmission by body louse (vector)
* Reservoir --\> humans + flying squirrels
207
Brill-Zinsser
Relapse of epidemic typhus. Can appear 10-40 years later
208
Cause of Murine Typhus (Endemic Typhus)
What are its clinical manifestations?
R. Typhi
_Manifestations_: Abrupt fever, severe headache, chills, myalgia. Late rash in 50% of cases
209
Endemic Typhus Epidemiology (vectors, reservoirs, where is it found?
_Vectors_: Rat flea; cat flea __
_Reservoirs_: Rodents
Found in temperate and subtropical coastal areas
210
Cause of Scrub Typhus.
Clinical Manifestations
Orientia tsutsugamushi
_Manifestations_: Maculopapular rash after 5 days, lymphadenopathy; fever; headache. Necrotic eschar 50-80% of the time.
211
Epidemiology of Scrub Typhus (location, vector/reservoir, spread)
(caused by orientia tsutsugamushi)
Found in the Far East (southwest pacific, southeast asia, japan)
Mites are the vectors and reservoir
Passaged to progeny via infected ova
212
What are the 2 types of Ehrlichiosis? What is different between them?
Human anaplasmosis (HA) and Human monocyte ehrlichiosis (HME)
_HA:_ granulocytes primarily infected (Neutrophils, eosinophils, basophils)__
_HME_: monocytes, mononuclear phagocytes
213
Pathology and clinical manifestation (7) of Ehrlichiosis
Name the 2 bodies. What does this smaller body assemble?
_Pathology_: Infect circulating leukocytes; 2 polymorphic forms (smaller **elementary bodies** and larger **reticulate bodies**)
Elementary bodies assemble **_morulae_**
_Manifestations_: Flu-like illness; high fever; headache; typically no rash; leukopenia; thrombocytopenia; elevated serum transaminases (sometimes late onset)
214
Cause and Clinical manifestation of Q-fever
Coxiella burnetii
* _Clinical features_: Most human infections are NOT apparent. **_No rash_**. Mild, dry cough and pneumonia; abrupt onset of fever, chills, headache at 9-20 days.
* Resistant to drying; growth at low pH
* Fatalities are rare; subacute endocarditis is rare
215
Epidemiology of Q-fever (transmission, carriers, geographic distribution)
Transmission from animals to humans by inhalation of (fecal) dust.
Carried by large mammals (cattle, sheep, goats, etc.)
World-wide distribution
216
The key spore forming Gram Positive Anaerobes (4 ) hint: all are related
1. Clostridum perfringens
2. Clostridium tetani
3. Clostridium botulinum
4. Clostridium difficle
217
What are the 3 disease that are affliated with Clostridium perfringens?
1. Gas gangrene (classically affliated)
2. Intraabdominal infections
3. Food poisoning
218
Strucure of C. perfringens (gram status, motility, encaspulation, spore status, hemolytic status, shape)
–Gram positive, "box car" shaped
–Non-motile
–Encapsulated
–Forms spores
–Double zone hemolysis
219
Gas Gangrene (pathogenesis, clinical presentation, treatment)
_Pathogenesis_: Trauma with devitalized tissue/muscle; spores from C. perfringens (and other bacteria) enter, germinate and quickly release toxins (alpha and iota)
_Clinical manifestation_: rapid onset; necrosis; bullae formation; crepitis (skin pops upon palpation)
_Treatment_: ****DEBRIDEMENT**
220
Main type of C. perfringens involved in Gas gangrene and its main associated toxins (2)
Type A is the most common cause
_Alpha and Iota Toxins_ are the most key
**Alpha**- lysis of inflammatory cells (white cells) and tissue destruction
**Iota**- necrosis and vascular permeability
221
Clostridium tetani pathogenesis + clinical manifestation
Spores enters via puncture wounds, burns, umbilicus etc. which bring it to an anaerobic environment.
There is local germination _without necrosis_
The tetanospasmin neurotoxin is the thing which has pathogenic effects
_**Clinical Manifestation**_: lock jaw, opsithotonus (classic full body flexion).
222
Treatment/ Prevention of Tetanus
Human tetanus immunoglobulin (HTIG) --\> binds up free toxin
Vaccine is available as well (every 10)
223
One of the most common ways that C. botulinum is delivered
Home canning of foods because the spores are extremely heat resistant so if you don't apply pressure + heat for a long time, preformed toxins may contaminate the food.
224
What is the most potent toxin in nature?
How does it work?
Clostridium botulinum
Blocks acetylcholine release by cleaving snares
225
What is distinct about the clinical presentation of Botulism?
What is the treatment for Botulism?
Descending paralysis, flaccid in nature
(cranial down)
Antitoxin + supportive treatment
226
The two key toxins of C. Dif
Toxin A (enterotoxin, inflammatory response, major toxin)
Toxin B (cytotoxic)
227
Clinical presentation of C. dif (6)
What is the dominate strain of C. dif in the US?
1. Pseudomembranous colitis
2. Diarrhea (watery/bloody)
3. Abdominal pain
4. **Leukocytosis**
5. Fever
6. Toxic megacolon (may require colectomy)
BI (Nap1) Strain = dominate in U.S.
228
Standard for C. dif detection
What is the treatment?
PCR (amplifies toxin region)
Very sensitive and specific
_Treated with **Vancomycin**_; sometimes colon resection or fecal transplant is needed; stop other antibiotics if possible
229
What is the main gram negative anaerobe?
Bacteroide fragilis
230
Necrosis and Clostridium tetani
You have local germination _without_ necrosis in C. tetani
231
Key clinical manifestations of B. fragilis
What types of infections are they commonly associated with?
Hallmark is _abscess formation_
This is almost always a mixed infection, filled with pus of PMN's, fibrin, and debris/necrotic tissue.
Most ofen associated with intraabdominal infection and in wound infection (skin and soft tissue)
232
What are the 2 most important aerobes and anaerobes we encounter clinically?
E.coli (aerobe) and B. fragilis (anaerobe)
233
(5) key differences between Bacteroides and Prevotella:
These are very similar and both only cause harm if they end up in the wrong place. Except unlike bacterioides, _Prevotella_...
1. has no virulence factors
2. normally lives in mouth and pelvis (instead of gut like bac.)
3. it has no dismutase so is less tolerant of oxygen
4. not encapsulated
5. doesn't get into bloodstream
234
Although it is an anaerobe, how are bacterioles able to survive if exposed to oxygen?
They have an oxygen toleronce due to super oxide dismutase and catalase presence.
235
Pathogenesis of Prevotella spp
Mixed _abscess_ is formed
236
What main Prevotella spp are associated with female genital tract infections? With oral/GU/GI tract infections?
_Genital tract infections_: P. bivia; P. disiens
_Oral/GU/GI_: P. melaninogenica
237
What are the 2 main types of Fusobacterium and what are their key clinical features?
1. **F. nucleatum**: spiration pneumonia and other lung diseases, brain and liver abscess, otitis media and sinusitis
2. **F. necrophorum**: Lemierre's syndrome (bacterial infection coasues abscess which leads to clot formation, embolis and sepsis); highly virulent (**potent endotoxin**)
238
Bacteroides are all resistant to what drug...
Which is why you must...
Penicillin
Must co-administer if penicillin family member is given (example ampicillin/ sulbactam)
239
The 3 main types of chlamydiaceae
Chlamydia (1. C. trachomatis)
Chlamydophila (2. C. psittaci; 3. C. pneumoniae)
240
Is Chlamydia intracellular or extracellular? Why? How does this play a role in its pathogenesis?
It is an obligate intracellular bacteria because it depends on the host cell for ATP.
The actual disease of chlamydia is based on it passing from cell to cell as elementary bodies that fill the cell until lysing and then pass onto other cells (causing inflammation)
241
A/B/C Immunotypes of C. trachomatis
Trachoma
Prevalent worldwide and causes follicular conjunctivitis, eyelid curling and scaring which leads to blindness. Major cause of blindness worldwide.
242
D-K serotypes of C. trachomatis
Common STD form
Leads to urethritis in males but is relatively asymptomatic for women (maybe cervicitis) which is why in can often lead to ovarian scarring and infertility.
243
What effects can serotype D-K of C. trachomatis have on neonates?
Chlamydia that the mom has can lead to infant pneumonia or neonatal conjunctivitis
244
L1,2,3 serotype of Chlamydia trachomatis info and clinical manifestations
Lymphogranuloma venereum
Often found in South America and Africa. Suppurative multilocular inguinal lymph nodes (bubos)
245
Main method of diagnosis for Chlamydia trachomatis. What doesn't this work for?
DNA probe of ribosomal RNA
Doesn't work will for LGV (serology is used)
246
Treatment of Chlamydia trachomatis
_Penicillin is not effective_ because of a **lack of peptidoglycan** for chlamydia species.
Other anti-biotics are given usually for 7 days (tetracyclines, quinolones, erythromycin); Azithromycin is a one and done dose.
This works for everything but **Lymphogranuloma** which requires a _3 week course._
247
What is missing from Chlamydia's cell wall?
NO _PEPTIDOGLYCANS!!!_
248
Cliical manifestations of C. pneumoniae
Can be pharyngitis, laryngitis or a **walking pneumonia**
249
Clinical Manifestation and Pathogenesis of C. psittaci
Caused by inhalation of respiratory secretions or droppings of infected _birds_ (usually exotic birds)
Leads to **lower respiratory infection**
250
Pathogenesis of mycoplasm pneumoniae
Attaches to clilia/ microvilli of bronchial epithelium and causes inflammatory response which can lead to walking pneumonia
251
Epidemiology of Mycoplasma pneumoniae
* Epidemics every 4-7 years
* Usually originates in young people and spreads among families
* One person is infected and just as they feel better someone else shows symptoms (due to incubation period)
252
Staining of Legionella
Technically gram-negative but does not stain well. Requires silver stain to be visible.
253
What is the most common Legionella serotype?
Serotype 1
254
What is the key cultural characteristic of Legionella? How does this effect its treatment.
It is beta-lactamase positive so no penicillin drugs will be useful.
255
Epidemiology of Legionella (where is it found? who does it effect most?)
Lives in water and is often in aquatic lakes or man-made reservoirs. Can be found in potable water systems because it survives in biofilms.
Often healthcare associated and specifcally has a heavier effect on unhealthy people (organ recipients, cigarette smokers, chronic lung disease)
256
Pathogenesis of Legionella. What are the 2 main clinical manifestations?
It is inhaled and uses a porin to bind to complement receptors and become endocytosed so that it can multiply intracellular.
1. _Pontiac Fever_- febrile influenza-like illness **w/o** respiratory component. Short incubation and self-limited.
2. _Legionellosis_- very **severe pneumonia**. Longer incubation and multilobar with ability to reach multiple systems
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Special media for culturing Legionella
Buffered charcoal yeast extract agar (BYCE)
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Test for diagnosis of Legionella
Urinary antigen test can be used specifically to test for the _serogroup 1_ type of legionella (because this is most common). Not definitive because there are other serotypes.
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Main treatments for Legionella
Macrolides or Fluoroquinolones
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What are the 2 bacteria species that form spores
1. Bacillus
2. Clostridium
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4 major virulence factors for Enterobacteriaceae
* Endotoxins
* Capsule
* Antigenic Phase Variation
* Type IIIsecretion systems
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Treatment of Salmonella
Third Generation Cephalosporin
